Transplantation of mesenchymal stem cells attenuates myocardial injury and dysfunction in a rat model of acute myocarditis

Treatment of experimental arthritis by inducing immune tolerance with human adipose‐derived mesenchymal stem cells

“…Moreover, human AD-MSCs have been shown to inhibit the secretion of various inflammatory cytokines by monocytes isolated from RA patients and macrophages from mice with colitis (24,39). Several studies have also shown that BM-MSCs and AD-MSCs of murine origin are able to down-regulate systemic and local inflammatory responses (11,(14)(15)(16)(17)(18). However, the specific molecular mechanisms involved are not yet fully understood.…”

“…Besides their capacity to differentiate into mesenchymal and nonmesenchymal cell lineages (7,8) and their potential clinical application for the repair of damaged tissues, several recent studies have shown that bone marrow-derived MSCs (BM-MSCs) regulate the immune response, including in vitro inhibition of T cell proliferation, B cell function, and dendritic cell maturation (9)(10)(11)(12)(13). Some researchers have reported the use of BM-MSCs to treat allograft rejection and acute graftversus-host disease as well as to alleviate experimental autoimmune encephalomyelitis, collagen-induced arthritis (CIA), and autoimmune myocarditis (11,(14)(15)(16)(17)(18)(19)(20). However, the specific molecular and cellular mechanisms involved in the immunoregulatory activity of BM-MSCs remain a subject of controversy.…”

Padrão de distribuição de células mononucleares de medula óssea em tecido cardíaco sadio por diferentes vias de infusão

“…A maioria dos estudos para o tratamento do infarto do miocárdio emprega a utilização de células adultas, como o mioblasto esquelético 6,7 , de células mesenquimais [8][9][10] , e de células mononucleares da medula óssea, obtidas por meio de punção da medula óssea 11 .…”

Cellular Therapy for Cardiovascular Disease Part 2—Delivery of Cells and Clinical Experience

“…This may account for the observation that patients with non-ischemic cardiomyopathy may have higher levels of CD34 + EPCs in peripheral blood, as in the absence of cardiac homing signals these cells fail to migrate and incorporate into the myocardium to assist with endogenous repair. Preclinical data in non-ischemic cardiomyopathy has focused on small animal models of toxic (doxorubicin-induced) or genetic cardiomyopathy, with promising results demonstrated for both SkMs and BM-derived cells (Agbulut et al 2003;Kondoh et al 2007;Ohnishi et al 2007). Recently, myoblast transplantation also achieved functional benefi t in an ovine model of cardiomyopathy, induced by intracoronary doxorubicin (Borenstein et al 2007).…”